Dietary supplements coenzyme

Dietary supplements For migraines, scientific data show a substantial health benefit for magnesium and Vitamin B. Contradictory, insufficient, or preliminary studies suggest a health benefit or minimal health benefit for 5-HTP, Coenzyme QIO, and Vitamin Bj2... 

As a dietary supplement, 30 mg of coenzyme Q10 is adequate to replace low endogenous levels. For cardiac effects, typical dosages are 100-600 mg/d given in two or three divided doses. These doses increase endogenous levels to 2-3 mcg/mL (normal for healthy adults, 0.7-1 mcg/mL). 

There has been some interest in raising the concentration of ot-locopherol, p-carotene, and ubiquinol (reduced coenzyme Q) in the LDL particle by dietary supplements, with the hope of reducing oxidative damage to its lipids and to apo A. There has also been some interest in raising plasma ascorbate for the same purpose. Studies with humans have revealed that the lev els of a-locophcrol and ubiquinol inside the LDL particle can be increased by two to fourfold, by dietary moans (Kaydenand Traber, 1993 Jialal and Grundy, 1992, Thomas e/ ai., 1995, Furr and Clark, 1997). 

Coenzyme QIO is a powerful antioxidant naturally occurring in the mitochondria of myocardium, and it is an electron carrier in the mitochondrial synthesis of ATP. Patients with heart failure have lower myocardial levels of coenzyme QIO, but supplementation has been demonstrated to have variable benefits in randomized controlled trials. One meta-analysis on the use in congestive heart failure showed improvements in stroke volume, ejection fraction, cardiac output, cardiac index, and end diastolic volume index. " Another antioxidant associated with beneficial effects in cardiac patients is lycopene, a natural constituent of tomatoes. Lycopene is the major carotenoid found in human serum, and epidemiological studies have indicated an effect of dietary supplementation in reducing heart disease. Few dietary interventions have been reported one study showed a mild but significant hypocholesterolemic effect, and another showed a significant reduction in LDL oxidation. " Animal studies show an antiatherogenic effect of DHEA, and a review of the clinical trials and studies on DHEA in males with coronary heart disease reported a favorable or neutral effect. Plasma levels of DHEA are decreased in patients with chronic heart failure in proportion to its severity. ... 

Vitamin B complex is the collective term for a number of water-soluble vitamins found particularly in dairy products, cereals and liver.Vitamin B (thiamine) is used by mouth for dietary supplement purposes and by injection in emergency treatment of Wernicke-Korsakoff syndrome. Vitamin B2 (riboflavin) is a constituent of the coenzyme FAD (flavine adenine dinucleotide) and FMN (flavine mononucleotide) and is therefore important in cellular respiration. Vitamin Be (pyridoxine) is a coenzyme for decarboxylases and transamination, and is concerned with many metabolic processes. Overdose causes peripheral neuropathy. It may be used medically for vomiting and radiation sickness and for premenstrual tension. Pyridoxine has a negative interaction with the therapeutic use of levodopa in parkinsonism by enhancing levodopa decarboxylation to dopamine in the periphery, which does not then reach the brain. The antitubercular drug isoniazid interferes with pyridoxine, and causes a deficiency leading to peripheral neuritis that may need to be corrected with dietary supplements. Vitamin B ... 

The answer is c. (Murray, pp 123-148. Scriver, pp 2367-2424. Sack, pp 159-175. Wilson, pp 287-317.) The most likely cause of the symptoms observed is carnitine deficiency. Under normal circumstances, long-chain fatty acids coming into muscle cells are activated as acyl coenzyme A and transported as acyl carnitine across the inner mitochondrial membrane into the matrix. A deficiency in carnitine, which is normally synthesized in the liver, can be genetic but it is also observed in preterm babies with liver problems and dialysis patients. Blockage of the transport of long-chain fatty acids into mitochondria not only deprives the patient of energy production, but also disrupts the structure of the muscle cell with the accumulation of lipid droplets. Oral dietary supplementation usually can effect a cure. Deficiencies in the carnitine acyltransferase enzymes I and II can cause similar symptoms. 

Immediate treatment with large doses (50-KX) mg) of intravenous thiamine may produce a measurable decrease in cardiac output and increase in peripheral vascular resistance as early as 30 minutes after the initial injection. Dietary supplementation of thiamine is not as effective because ethanol consumption interferes with thiamine absorption. Because ethanol also affects the absorption of most water-soluble vitamins, or their conversion to the coenzyme form, Al Martini was also given a bolus containing a multivitamin supplement. 

Nicotinic acid is a B-complex vitamin that is converted to nicotinamide, NAD, and NADP. The latter two compounds are coenzymes and are required tor oxidation/reduction reactions in a variety of biochemical pathways. Additionally, nicotinic acid is metabolized to a number of inactive compounds, including nicotinuric acid and N-methylated derivatives. Normal biochemical regulation and feedback prevent large doses of nicotinic acid from producing excess quantities of NAD and NADP. Thus, small doses of nicotinic acid, such as those used tor dietary supplementation, will be primarily excreted as metabolites, whereas large doses, such as those used tor the treatment of hyperlipoproteinemia, will be primarily excreted unchanged by the kidney (15). 

One study involving breast cancer patients showed that CoQlO concentrations in tumor tissues were significantly depleted compared with the surroimding normal tissues. Administration of coenzyme QIO by dietary supplementation may induce a protective effect on breast tissue. ... 

Rich sources of dietary coenzyme Qio include mainly meat, poultry, and fish. Other relatively rich sources include soybean and canola oils, and nuts. Fruits, vegetables, eggs, and dairy products are moderate sources of coenzyme Qio. Coenzyme Qio is also available without a prescription as a dietary supplement. 

Vitamin B12 must be converted into its coenzyme forms, adenosylcobalamin and methylcobalamin, in the cell. These coenzymes function as cofactors of methylmalonyl-CoA mutase and methionine synthase, respectively. Chronic kidney disease (CKD) may affect the conversion from vitamin B12 to the coenzyme forms. This section describes the intracellular metabolism of cyanocobalamin, which is included in many dietary supplements, in particular, referring to a recently discovered trafficking chaperone called methylmalonic aciduria cdlC type with homocystinuria (MMACHC). Cyanocobalamin is first converted to cob(II)alamin, which has no cyanogen group on the ligand occupying the upper axial position of the cobalamin structure. Cob(II)alamin is further reduced to cob(I)alamin, which can function as a coenzyme in the body. 

The curative material, which is abundant in green leafy vegetables, was named folic acid. However, this name is usually reserved for the synthetic compound used in dietary supplementation. The natural forms are largely the coenzymes (Fig. 6), which are collectively called folates. The last of the accepted human vitamins to be discovered was vitamin Bn. A cobalt-containing organic compound needed in very small amounts, it cures and prevents pernicious anemia, which was often a fatal disease of people over 60 years of age. Its complex structure (Fig. 7) was determined by X-ray diffraction after numerous efforts at chemicai characterization had failed. However, cy anocobalamin, the compound isolated and the form used in nutritional supplementation, is an artifact of the isolation and synthesis. The natural vitamin may have OH in place of CN but consists largely of the coenzyme forms. 

Co Cobaltamin S Coenzyme vitamin Bi2 Dietary vitamin supplement... 

If folate is given without cobalamin to a B 12-deficient patient, the drug only partially corrects the megaloblastic anemia because it will bypass the methyl-folate trap and provide adequate FH4 coenzyme for the conversion of dUMP to dTMP and for a resurgence of purine synthesis. As a result, normal DNA synthesis, DNA repair, and cell division occur. However, the neurologic syndrome, resulting from hypomethylation in nervous tissue, may progress unless the physician realizes that B12 supplementation is required. In Jean Ann s case, in which the serum B12 concentration was borderline low and in which the dietary history supported the possibility of a B12 deficiency, a combination of folate and B12 supplements is required to avoid this potential therapeutic trap. 

Treatment in those patients who respond to pyridoxal phosphate is based on provision of approximately 250-500 mg per day. Folate deficiency may be avoided by the addition of 5 mg per day to this regimen. In patients who do not respond to the coenzyme, dietary manipnlation with a low methionine, cystine-supplemented diet may be helpfnl. Dipyridamole, an agent effective in decreasing platelet aggregation, has been nsed to prevent the thromboses, but there are no reports yet as to its effectiveness. 

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